Evidence map›Paper›PMID 29882812›Full record

ReviewInternational journal of molecular sciences2018

Pharmacological Targeting of Cell Cycle, Apoptotic and Cell Adhesion Signaling Pathways Implicated in Chemoresistance of Cancer Cells.

Dauren Alimbetov, Sholpan Askarova, Bauyrzhan Umbayev, Terence Davis, David Kipling

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Murine Cell Line Models for Vascular Mimicry: The Role of YAP/TAZ Signaling.International journal of molecular sciences · 2025
    Article
  9. Review
  10. Article
  11. Gintonin-EnrichedFoods (Basel, Switzerland) · 2025
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Synthesis and Preclinical Evaluation of NovelACS medicinal chemistry letters · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Article

13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Dauren AlimbetovLaboratory of bioengineering and regenerative medicine, Center for Life Sciences, National Laboratory Astana, Nazarbayev University, 53 Kabanbay Batyr Ave, Z05H0P9 Astana, Kazakhstan. dauren.alimbetov@nu.edu.kz.
Sholpan AskarovaLaboratory of bioengineering and regenerative medicine, Center for Life Sciences, National Laboratory Astana, Nazarbayev University, 53 Kabanbay Batyr Ave, Z05H0P9 Astana, Kazakhstan. shaskarova@nu.edu.kz.ORCID 0000-0001-6161-1671
Bauyrzhan UmbayevLaboratory of bioengineering and regenerative medicine, Center for Life Sciences, National Laboratory Astana, Nazarbayev University, 53 Kabanbay Batyr Ave, Z05H0P9 Astana, Kazakhstan. bauyrzhan.umbayev@nu.edu.kz.ORCID 0000-0002-0286-7252
Terence DavisDivision of Cancer and Genetics, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK. davist2@Cardiff.ac.uk.ORCID 0000-0003-2780-0262
David KiplingDivision of Cancer and Genetics, Cardiff University School of Medicine, Heath Park, Cardiff CF14 4XN, UK. kiplingd@cardiff.ac.uk.
Nazarbayev University · KZCardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapeutic drugs target a physiological differentiating feature of cancer cells as they tend to actively proliferate more than normal cells. They have well-known side-effects resulting from the death of highly proliferative normal cells in the gut and immune system. Cancer treatment has changed dramatically over the years owing to rapid advances in oncology research. Developments in cancer therapies, namely surgery, radiotherapy, cytotoxic chemotherapy and selective treatment methods due to better understanding of tumor characteristics, have significantly increased cancer survival. However, many chemotherapeutic regimes still fail, with 90% of the drug failures in metastatic cancer treatment due to chemoresistance, as cancer cells eventually develop resistance to chemotherapeutic drugs. Chemoresistance is caused through genetic mutations in various proteins involved in cellular mechanisms such as cell cycle, apoptosis and cell adhesion, and targeting those mechanisms could improve outcomes of cancer therapy. Recent developments in cancer treatment are focused on combination therapy, whereby cells are sensitized to chemotherapeutic agents using inhibitors of target pathways inducing chemoresistance thus, hopefully, overcoming the problems of drug resistance. In this review, we discuss the role of cell cycle, apoptosis and cell adhesion in cancer chemoresistance mechanisms, possible drugs to target these pathways and, thus, novel therapeutic approaches for cancer treatment.

Indexed as

Drug Resistance, NeoplasmAnimalsAntineoplastic AgentsApoptosisCell AdhesionCell Adhesion MoleculesCell CycleHumansMolecular Targeted TherapyNeoplasmsSignal TransductionTransforming Growth FactorsAntineoplastic AgentsCell Adhesion MoleculesTransforming Growth Factorsapoptosiscell adhesioncell cyclechemoresistancesmall molecules

Identifiers

PMID29882812
PMCPMC6032165
OpenAlexW2806296092

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.